Non-steroidal anti-inflammatory drugs (NSAIDs) as a hidden threat to scavenging raptors beyond Gyps: A call for wider research and surveillance

IF 4.2 3区环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES

Environmental toxicology and pharmacology Pub Date : 2025-09-09 DOI:10.1016/j.etap.2025.104817

Kane Colston , Karen Mifsud , Nicola Rooney , Juan Manuel Grande , Irene Bueno

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Abstract

Asian vulture declines have been linked to the consumption of contaminated livestock carcasses with the non-steroidal anti-inflammatory (NSAID) diclofenac. Studies have suggested that the toxicity of NSAIDs to Old World vultures may be through an intronic premature termination codon (PTC) in the gene CYP2C19, encoding a cytochrome P450 enzyme thought responsible for diclofenac metabolism in vultures. However, it remains unclear whether this mechanism applies for all susceptible raptor species. We used nucleotide databases (NCBI) to compare the Cape vulture (Gyps coprotheres) CYP2C19 sequence to other vulture sequences to identify the presence of the intronic PTC. Our search revealed that only Gyps species possessed the CYP2C19 PTC. This is despite NSAID toxicity at similar contaminant levels found in non-Gyps accipitrid mortalities. Our findings suggest avian scavengers could be affected by additional toxicological mechanisms, including sublethal toxicity. Further research is required to establish such mechanisms and exposure risk in non-Gyps scavengers.

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非甾体抗炎药（NSAIDs）对食腐猛禽的潜在威胁：呼吁进行更广泛的研究和监测

亚洲秃鹫数量的减少与食用含有非甾体抗炎药（NSAID）双氯芬酸的受污染牲畜尸体有关。研究表明，非甾体抗炎药对东半球秃鹫的毒性可能是通过基因CYP2C19中的内含子过早终止密码子（PTC）产生的，该基因编码一种细胞色素P450酶，被认为与秃鹫的双氯芬酸代谢有关。然而，尚不清楚这种机制是否适用于所有易感猛禽物种。我们使用核苷酸数据库（NCBI）将Cape vulture (Gyps coprothers) CYP2C19序列与其他秃鹫序列进行比较，以确定内含子PTC的存在。我们的研究发现，只有Gyps物种具有CYP2C19 PTC。尽管非吉卜赛人的非甾体抗炎药毒性与非吉卜赛人的急性死亡率相似。我们的研究结果表明，鸟类食腐动物可能受到其他毒理学机制的影响，包括亚致死毒性。需要进一步的研究来确定这种机制和非gyps食腐动物的暴露风险。

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来源期刊

Environmental toxicology and pharmacology 医学-毒理学

CiteScore

7.00

自引率

4.70%

发文量

185

审稿时长

34 days

期刊介绍： Environmental Toxicology and Pharmacology publishes the results of studies concerning toxic and pharmacological effects of (human and veterinary) drugs and of environmental contaminants in animals and man. Areas of special interest are: molecular mechanisms of toxicity, biotransformation and toxicokinetics (including toxicokinetic modelling), molecular, biochemical and physiological mechanisms explaining differences in sensitivity between species and individuals, the characterisation of pathophysiological models and mechanisms involved in the development of effects and the identification of biological markers that can be used to study exposure and effects in man and animals. In addition to full length papers, short communications, full-length reviews and mini-reviews, Environmental Toxicology and Pharmacology will publish in depth assessments of special problem areas. The latter publications may exceed the length of a full length paper three to fourfold. A basic requirement is that the assessments are made under the auspices of international groups of leading experts in the fields concerned. The information examined may either consist of data that were already published, or of new data that were obtained within the framework of collaborative research programmes. Provision is also made for the acceptance of minireviews on (classes of) compounds, toxicities or mechanisms, debating recent advances in rapidly developing fields that fall within the scope of the journal.